Dual diagnosis is a term commonly employed in substance use disorder (SUD) treatment. What is less recognizable is the concept of disturbed sleep as a co-occurring disorder in need of management.

As is the case with affective and anxiety disorders, a growing body of evidence is emerging that SUDs share a complicated relationship with sleep that is bidirectional. Findings suggest that a history of baseline insomnia may be predictive of disordered substance use.1,2 It is also interesting that abstinent adolescents with a family history of substance dependence are more likely to experience difficulties sleeping—a fact that may illustrate psychosocial factors or the presence of a genetic association between sleep and SUDs.

Recent evaluations indicate that polymorphisms of clock genes elucidate this association. Clock genes encode for proteins that form part of an auto-regulatory feedback loop that cycles over a 24-hour period. Variations in certain Clock genes appear to influence sleep drive and circadian preferences; one such gene, PER 3, has been linked to insomnia severity in alcoholic patients.3 New frontiers in addiction research have also implicated neuropeptides such as orexin in the dual role of sleep and reward circuitry.4 The lateral hypothalamus contains many of the neurotransmitters and neural networks involved in alertness, concentration, mood, and regulation of the sleep-wake cycle; many of these networks extend to the reward center that is manipulated by substances of abuse.

It may not come as a surprise that while 10% to 15% of the general population experiences insomnia, reports for subjects with active alcohol use disorders and comorbid sleep disturbance range from 30% to 80%.5 Sleep disruption complicates acute withdrawal as well—upwards of 50% of patients report sleep disturbance during acute withdrawal from alcohol.6 Sleep disturbance in early recovery also represents a formidable obstacle for patients with alcohol use disorder; a subset of patients experiences first-episode insomnia with sobriety. While recovery of restorative sleep is possible with sobriety, it has been suggested that disordered sleep may persist for years in people with a history of chronic alcohol use and increases vulnerability to relapse.

Sleep disturbances and relapse risk

Users who perceive their substance of abuse as soporific may be at increased risk for sleep disturbances and relapse. This perception may be based on early experiences of the substance, when moderate use of alcohol may indeed have conferred subjective sleep benefits such as reduced onset to sleep. A recent analysis that looked at the link between sleep disturbance and alcohol relapse in a residential treatment facility suggests that patients who reported use of alcohol as a sleep aid were more than 3-fold more likely to relapse at 12 months (odds ratio [OR] = 3.26; 95% confidence interval [CI] = 1.33-7.95; P = .008).7 Study findings also indicate a significant association between patients’ use of hypnotics at admission and alcohol relapse at 12 months (OR = 4.03; 95% CI = 1.63-9.97; P = .002).

Foster et al8 queried alcohol-dependent subjects in an inpatient setting and found a subjective sense of sleep latency to be a predictor of relapse. Other studies also support this association between subjective perceptions of increased awakenings and difficulty falling asleep and relapse risk in early alcohol recovery.

Objective evidence of sleep disturbance exists in alcohol use disorders as well. Polysomnography studies suggest that chronic alcohol use increases sleep latency (defined as the amount of time from lights out to sleep onset) throughout the vacillating stages of use, including active drinking periods, acute withdrawal, post-withdrawal, and early and late recovery. In their review, Angarita and colleagues9 conclude that total sleep time (the amount of sleep in one complete episode of sleeping) is uniformly adversely affected by alcohol in all of its use stages from active drinking to later recovery.

Persons with alcohol use disorders also appear to suffer from slow wave sleep deficits (stage N3), which may correspond to difficulty with learning, memory, and cognitive performance. Use of alcohol results in suppression of REM sleep. Following 2 to 3 weeks of abstinence, there appears to be a REM rebound, which some patients describe as an increase in vivid dreams.